ArticleIn vitro cellular & developmental biology. Animal2026
RYK silencing-modified bone marrow-derived mesenchymal stem cells suppress gastric cancer progression.
Article in In vitro cellular & developmental biology. Animal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- The multifaceted roles of receptor tyrosine pseudokinases in cellular signalling.Biochemical Society transactions · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
Gastric cancer (GC) is a prevalent malignant tumor threatening human health. This study aimed to explore the potential mechanism of receptor-like tyrosine kinase (RYK) silencing-modified bone marrow-derived mesenchymal stem cells (BMSCs) in the progression of GC. BMSCs were transfected with the RYK siRNA and negative controls. Cell co-culture experiments were used to explore the interaction between different BMSCs and human gastric carcinoma cell line NCI-N87. Cancer cell proliferation, cell cycle, apoptosis, colony formative ability, and invasive ability were assessed. Western blot analysis was performed to determine the protein levels of cyclinA, Bcl-xL, Bcl-2, cleaved caspase 3, cleaved caspase 7, cleaved caspase 9, and cleaved PARP1 in NCI-N87 cells. Compared with NCI-N87 cells, co-culture of si-NC-modified BMSCs with NCI-N87 cells promoted the proliferation, colony formative ability, and invasion of NCI-N87 cells, inhibited the apoptosis of NCI-N87 cells, and reduced the proportion of NCI-N87 cells present in G2/M phase cells. In addition, compared with the si-NC-BMSCs + N87 group, the si-RYK-BMSCs + N87 group inhibited the proliferation, colony formative ability, and invasion of NCI-N87 cells, promoted the apoptosis of NCI-N87 cells, and increased the proportion of G2/M phase cells. Thus, RYK silencing-modified BMSCs can inhibit the proliferation, colony formative ability, and invasion of NCI-N87 cells, while inducing apoptosis and G2/M phase arrest.
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Registered trials
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